Recent advances in basic research on the trigeminal ganglion

被引：30

作者：

Goto, Tetsuya ^{[1
]}

Oh, Seog Bae ^{[2
]}

Takeda, Mamoru ^{[3
]}

Shinoda, Masamichi ^{[4
]}

Sato, Tadasu ^{[5
]}

Gunjikake, Kaori K. ^{[6
]}

Iwata, Koichi ^{[4
]}

机构：

[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Oral Anat & Cell Biol, Kagoshima 8906544, Japan

[2] Seoul Natl Univ, Sch Dent, Dept Neurobiol & Physiol, Seoul, South Korea

[3] Azabu Univ, Sch Life & Environm Sci, Dept Food & Life Sci, Sagamihara, Kanagawa, Japan

[4] Nihon Univ, Sch Dent, Dept Physiol, Tokyo, Japan

[5] Tohoku Univ, Grad Sch Dent, Div Oral & Craniofacial Anat, Sendai, Miyagi, Japan

[6] Kyushu Dent Univ, Sch Dent, Dept Orthodont, Kitakyushu, Fukuoka, Japan

来源：

JOURNAL OF PHYSIOLOGICAL SCIENCES | 2016年 / 66卷 / 05期

关键词：

Trigeminal ganglion; Neuron; Satellite glial cell; Hyperalgesia; Allodynia; Pain; SATELLITE GLIAL-CELLS; ENHANCED EXCITABILITY; MECHANICAL ALLODYNIA; POTASSIUM CURRENTS; SENSORY GANGLIA; NEURONS; ACTIVATION; AFFERENT; RECEPTORS;

D O I：

10.1007/s12576-016-0448-1

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Peripheral tissue inflammation can alter the properties of somatic sensory pathways, causing behavioral hypersensitivity and resulting in increased responses to pain caused by noxious stimulation (hyperalgesia) and normally innocuous stimulation (allodynia). These hypersensitivities for nociception are caused by changes in the excitability of trigeminal ganglion (TG) neurons. These changes alter sensory information processing in the neurons in the medullary trigeminal nucleus of caudalis. Increasing information is becoming available regarding trigeminal neuron-neuron/neuron-satellite glial cells (SGCs) communication. The activation of intraganglionic communication plays an important role in the creation and maintenance of trigeminal pathological pain. Therefore, in this review, we focus on the recent findings for sensory functions and pharmacological modulation of TG neurons and SGCs under normal and pathological conditions, and we discuss potential therapeutic targets in glia-neuronal interactions for the prevention of trigeminal neuropathic and inflammatory pain.

引用

页码：381 / 386

页数：6

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